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Pharmacology > Diuretics > Flashcards

Diuretics Flashcards

1
Q

What is the primary function of diuretics? What do they treat (generally)?

A

Increase volume of urine

Treats edema

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2
Q

From what drug were the first diuretics all derived?

A

Sulfonilamide

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3
Q

What kinds of conditions can lead NaCl intake to exceed output?

A

CHF or Renal Failure

Leads to edema

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4
Q

About what % of NaCl is reabsorbed in the PCT?

A

65%

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5
Q

About what % of NaCl is reabsorbed in the thin descending limb?

A

0%

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6
Q

About what % of NaCl is reabsorbed in the thick ascending limb?

A

35%

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7
Q

About what % of NaCl is reabsorbed in the DCT?

A

10%

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8
Q

About what % of NaCl is reabsorbed in the collecting duct?

A

2-5%

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9
Q

How do most diuretics get into the luminal fluid? What is the exception?

A

Most reach the luminal fluid by organic acid and base secretion in the PCT. They are not filtered at the glomerulus because they are protein bound.

Mannitol is the exception and it is filtered at the glomerulus.

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10
Q

What transporters are present on the basal side of the PCT epithelium?

A

Na+/K+ ATPase

Na+/HCO3- cotransporter

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11
Q

Acetazolamide

MOA

A

Reversible inhibition of carbonic anhydrase

Inhibits reabsorption of HCO3- in the PCT

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12
Q

Acetazolamide

Adverse Effects

A

Metabolic acidosis (prevents HCO3- reabsorption into blood)

Hypokalemia

Calcium phosphate stones (decrease pH of the luminal fluid)

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13
Q

Acetazolamide

Contraindication

A

Cirrhosis

Increased urine pH leads to less NH3 excretion, therefore giving higher NH3 serum levels

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14
Q

List the four carbonic anhydrase inhibitors

A

Acetazolamide
Dichlorphenamide
Methazolamide
Dorzolamide

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15
Q

Acetazolamide

Clinical Uses

A

Diuretic (pretty weak)

Glaucoma (reduces intraocular pressure)

Urinary alkalinization

Acute mountain sickness (prophylaxis – decrease hemoglobin’s affinity for O2 so more O2 is deposited at tissues)

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16
Q

Mannitol is what kind of diuretic?

Where does mannitol have its major effects?

A

Osmotic Diuretic

Major effects in the PCT, descending limb of loop of Henle, collecting ducts (if ADH present)

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17
Q

How does mannitol reach the luminal fluid?

A

Gets filtered at the glomerulus.

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18
Q

Mannitol

Administration

A

IV only

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19
Q

Mannitol

Adverse Effects

A

Increased plasma osmolality
Moves water out of the cells into the ECF, which can worsen heart failure
Acute pulmonary edema
Dehydration

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20
Q

Mannitol

Clinical Indications

A

Maintain or increase urine volume
Could treat acute renal failure
Reduce intracranial pressure
Reduce intraocular pressure

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21
Q

Mannitol

Contraindications

A

CHF
Chronic Renal failure
Pulmonary edema

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22
Q

What transporter is present on the apical membrane of the thick ascending limb?

A

Na+/K+/Cl- cotransporter

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23
Q

Action of the Na+/K+/Cl- cotransporter helps cause paracellular transport of what substances in the thick ascending limb?

A

Mg2+ and Ca2+

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24
Q

What is the primary mechanism of action for loop diuretics?

A

Inhibit the Na+/K+/Cl- cotransporter

Vasodilation – increase renal blood flow (prostaglandin mediated)

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25
Q

Furosemide

MOA

A

Inhibit the Na+/K+/Cl- cotransporter
Renal vasodilation
Decreases reabsorption of Mg2+ and Ca2+

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26
Q

Furosemide

Pharmacokinetics

A

Short half life (1-1.5 hrs)

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27
Q

Furosemide

Adverse Effects

A 
Hyponatremia
Hypokalemia
Hypomagnesemia
Metabolic alkalosis
Ototoxicity
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28
Q

Furosemide

Clinical Indications

A

Acute Pulmonary Edema
Edema assoc. with CHF
Acute hypercalcemia
Acute hyperkalemia

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29
Q

List the 4 Loop Diuretics

A

Furosemide
Bumetanide
Torsemide
Ethacrynic Acid

30
Q

Why is ethacrynic acid used as a last resort as a loop diuretic?

A

It is both nephrotoxic and ototoxic

31
Q

What channel is present on the distal convoluted tubule apical membrane?

A

Na+/Cl- cotransporter

32
Q

What channel is present on the distal convoluted tubule basolateral membrane? What receptor is present there?

A

Na+/K+ ATPase
Na+/Ca2+ antiporter (brings Na+ into cell and Ca2+ into blood)
PTH Receptor is also present on basolateral membrane

33
Q

Hydrochlorothiazide

MOA

A

Blocks the Na+/Cl- cotransporter on the apical membrane

Allows for more Ca2+ reabsorption

34
Q

Hydrochlorothiazide

Adverse Effects

A 
Hyponatremia
Hypokalemia
Metabolic alkalosis
Hyperglycemia
Hyperlipidemia
Dehydration
35
Q

Hydrochlorothiazide

Clinical Uses

A

HTN
CHF
Reduce Ca2+ excretion to prevent kidney stones

36
Q

List the thiazide diuretics

A 
Hydrochlorothiazide
Chlorothiazide
Metolazone
Indapamide
Chlorthalidone
37
Q

What channels are present on the apical membrane of principal cells of the collecting ducts?

A

Na+ channels (moving Na+ into the cell)
K+ channels (moving K+ out of the cell and into lumen)
H2O channels, bring H2O into cell

38
Q

Aldosterone binds its receptor where? What does that cause?

A

Binds receptors in principal cells of the collecting ducts.

Causes increased transcription of the Na+/K+ ATPase and apical Na+ channels

39
Q

Intercalated Cells contain what apical transporter? What is it regulated by?

A

H+ ATPase
Pumps H+ into the luminal fluid
Regulated by aldosterone

40
Q

How do Carbonic anhydrase inhibitors cause hypokalemia?

A

They cause an increased conc of Na+ and HCO3- to reach the collecting ducts, which leads to a greater negative luminal potential. This forces more K+ out of the cells into the lumen, thus wasting more K+ and causing hypokalemia

41
Q

How do thiazide and loop diuretics cause hypokalemia?

A

Cause an increased delivery of Na+ and Cl- to the collecting ducts, increasing the negative luminal potential in the collecting ducts and pulling more K+ out into the lumen. Causes hypokalemia (K+ wasting)

42
Q

How do thiazide and loop diuretics cause metabolic alkalosis?

A

Cause more Na+ and Cl- to reach the collecting ducts, thus increasing the negative luminal potential. Leads to more H+ being pumped out of intercalated cells by the H+ ATPase, thus causing metabolic alkalosis

43
Q

Where in the nephron do K+ sparing diuretics work?

A

Collectig tubules

44
Q

When should K+ sparing diuretics NEVER be given?

A

DO NOT use K+ sparing diuretics when hyperkalemia is a risk

DO NOT coadminister with an ACE inhibitor

45
Q

Spironolactone

MOA

A

Aldosterone receptor antagonist

Anti-androgenic effects

46
Q

Spironolactone

Adverse Effects

A 
Hyperkalemia
Metabolic acidosis
Gynecomastic, amenorrhea, impotence
GI Upset
CNS effects
47
Q

Spironolactone

Clinical Indications

A

Primary or Secondary Hyperaldosteronism
Liver cirrhosis – DOC
HTN

48
Q

Eplerenone

MOA

A

Aldosterone receptor antagonist

Does NOT have the same anti-androgenic effects that spironolactone does, so there are fewer side effects

49
Q

How can spironolactone cause metabolic acidosis?

A

Blocking aldosterone decreases the negative luminal potential.
Leads to less H+ efflux from the intercalated cells, so the H+ accumulates in the blood

50
Q

Amiloride

MOA

A

Blocks Na+ channels on principal cells

K+ sparing diuretic because it decreases driving force for K+ to leave cells

51
Q

Amiloride

Adverse Effects

A

Hyperkalemia

GI upsets
Muscle cramps
CNS effects

52
Q

Amiloride

Clinical Indications

A

Edema
HTN
Usually combined with a loop or thiazide diuretic to prevent K+ loss

53
Q

Triamterene

MOA

A

Blocks Na+ channels in principal cells

K+ sparing diuretic because it decreases driving force for K+ to leave cells

54
Q 
ADH Antagonists
What class of drugs is now used? List them and specify the receptor they antagonize
A

Vaptams

V2 receptor antagonists
Tolvaptam
Mozavaptam
Lixivaptam

V1a and V2 receptor antagonist
Conivaptam

55
Q

ADH Antagonists

Indications

A

SIADH
Euvolemic or hypervolemic hyponatremia
CHF

56
Q

ADH Antagonists

Adverse Effects

A 
Hypernatremia
Thirst
Dry mouth
Hypotension
Dizziness
57
Q

What kind of diuretic would you typically give for chronic right heart failure?

A

Oral Loop diuretic

58
Q

What kind of diuretic would you typically give for acute left heart failure?

A

IV Loop diuretic

You need aggressive and rapid therapy

59
Q

What is hyponatremia clinically defined as?

A

Serum Na+ concentration less than 136 mEq/L

60
Q

What kind of hyponatremia may be treated by administration of saline?

A

Hypovolemic hyponatremia

61
Q

What drugs are used to treat hyponatremia?

A

ADH receptor antagonists (Vaptams)

They increase serum Na+ conc and decrease urine osmolality

62
Q

What kind of diuretic should be used for uncomplicated HTN?

A

Thiazide diuretic

63
Q

For patients with diabetes and chronic kidney disease, what hypertensive medications should be used?

A

Two or more antihypertensive meds…

likely including a thiazide diuretic

64
Q

What is nephrogenic diabetes insipidus?

A

Loss of ADH effectivity in principal cells of the collecting tubules

65
Q

What diuretics should be used to treat nephrogenic diabetes insipidus? Why?

A

Thiazide diuretics

They may lead to increased Na+ channel synthesis and aquaporin synthesis in principal cells

66
Q

Kidney stones are mostly made of what?

A

Calcium

67
Q

Which diuretics are useful at preventing kidney stones? Why?

A

Thiazide diuretics are useful at preventing kidney stones because they increase the reabsorption of Ca2+.

68
Q

Which diuretics have an increased risk of causing kidney stones? Why?

A

Loop diuretics because they prevent the reabsorption of Ca2+, thus increasing Ca2+ concentration in the lumen of the nephron

69
Q

What diuretics should be used in hypercalcemia?

A

Loop diuretics (increase excretion of Ca2+)

70
Q

What diuretics should be avoided in hypercalcemia?

A

Thiazide diuretics (increase reabsorption of Ca2+)

Pharmacology (67 decks)

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